ArticlePLoS computational biology2013
Endogenous cholinergic inputs and local circuit mechanisms govern the phasic mesolimbic dopamine response to nicotine.
Article in PLoS computational biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- The alpha7 nicotinic acetylcholine receptor mediates network dysfunction in a mouse model of local amyloid pathology.Molecular psychiatry · 2026Article
- Article
- Cholinergic modulation of hierarchical inhibitory control over cortical resting state dynamics: Local circuit modeling of schizophrenia-related hypofrontality.Current research in neurobiology · 2021Article
- Neural circuits and nicotinic acetylcholine receptors mediate the cholinergic regulation of midbrain dopaminergic neurons and nicotine dependence.Acta pharmacologica Sinica · 2020Review
- Pharmacological Effects and Regulatory Mechanisms of Tobacco Smoking Effects on Food Intake and Weight Control.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018Review
- Minimal Circuit Model of Reward Prediction Error Computations and Effects of Nicotinic Modulations.Frontiers in neural circuits · 2018Article
- Altered nicotine reward-associated behavior following α4 nAChR subunit deletion in ventral midbrain.PloS one · 2017Article
- VTA dopamine neuron plasticity - the unusual suspects.The European journal of neuroscience · 2016Review
- Functional characterization of AT-1001, an α3β4 nicotinic acetylcholine receptor ligand, at human α3β4 and α4β2 nAChR.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2015Article
- Understanding the role α7 nicotinic receptors play in dopamine efflux in nucleus accumbens.ACS chemical neuroscience · 2014Article
- Co-activation of VTA DA and GABA neurons mediates nicotine reinforcement.Molecular psychiatry · 2013Article
- Article
- The Response of Ventral Tegmental Area Dopaminergic Neurons to Bupropion: Excitation or Inhibition?Basic and clinical neuroscienceArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nicotine exerts its reinforcing action by stimulating nicotinic acetylcholine receptors (nAChRs) and boosting dopamine (DA) output from the ventral tegmental area (VTA). Recent data have led to a debate about the principal pathway of nicotine action: direct stimulation of the DAergic cells through nAChR activation, or disinhibition mediated through desensitization of nAChRs on GABAergic interneurons. We use a computational model of the VTA circuitry and nAChR function to shed light on this issue. Our model illustrates that the α4β2-containing nAChRs either on DA or GABA cells can mediate the acute effects of nicotine. We account for in vitro as well as in vivo data, and predict the conditions necessary for either direct stimulation or disinhibition to be at the origin of DA activity increases. We propose key experiments to disentangle the contribution of both mechanisms. We show that the rate of endogenous acetylcholine input crucially determines the evoked DA response for both mechanisms. Together our results delineate the mechanisms by which the VTA mediates the acute rewarding properties of nicotine and suggest an acetylcholine dependence hypothesis for nicotine reinforcement.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.